An author was diagnosed with bipolar 1 disorder in 1985. She also blog for the Huffington Post and the International Bipolar Foundation. With this blog, she wants to tell story and to help other people with this illness, or any other mental illness.
Scientists have discovered “anxiety neurons” in the hippocampus of mice. They fire when mice are in anxiety provoking environments. And they can be silenced with light, at which time mice don’t exhibit anxious behavior any longer, but explore environments that would normally have been very anxiety provoking. Also these same cells can be activated with another setting of light and when that happens the mice exhibit very anxious behavior even in safe environments. And as of mice, so of men! So, hopefully this will lead to better treatments for anxiety for us humans. I’d be totally willing to be their guinea pig for new therapies for anxiety! I’ve been dealing with sometimes debilitating anxiety for at least two years now. Waiting for new treatments, as are a lot of others, I’m sure. Godspeed researchers!
We’re not wired to feel safe all the time, but maybe one day we could be.
A recent study investigating the neurological basis of anxiety in the brain has identified ‘anxiety cells’ located in the hippocampus – which not only regulate anxious behaviour but can be controlled by a beam of light.
The findings, so far demonstrated in experiments with lab mice, could offer a ray of hope for the millions of people worldwide who experience anxiety disorders (including almost one in five adults in the US), by leading to new drugs that silence these anxiety-controlling neurons.
“We wanted to understand where the emotional information that goes into the feeling of anxiety is encoded within the brain,” says one of the researchers, neuroscientist Mazen Kheirbek from the University of California, San Francisco.
To find out, the team used a technique called calcium imaging, inserting miniature microscopes into the brains of lab mice to record the activity of cells in the hippocampus as the animals made their way around their enclosures.
Anxiety cells (Hen Lab/Columbia University)
These weren’t just any ordinary cages, either.
The team built special mazes where some paths led to open spaces and elevated platforms – exposed environments known to induce anxiety in mice, due to increased vulnerability to predators.
Away from the safety of walls, something went off in the mice’s heads – with the researchers observing cells in a part of the hippocampus called ventral CA1 (vCA1) firing up, and the more anxious the mice behaved, the greater the neuron activity became.
“We call these anxiety cells because they only fire when the animals are in places that are innately frightening to them,” explains senior researcher Rene Hen from Columbia University.
The output of these cells was traced to the hypothalamus, a region of the brain that – among other things – regulates the hormones that controls emotions.
Because this same regulation process operates in people, too – not just lab mice exposed to anxiety-inducing labyrinths – the researchers hypothesise that the anxiety neurons themselves could be a part of human biology, too.
“Now that we’ve found these cells in the hippocampus, it opens up new areas for exploring treatment ideas that we didn’t know existed before,” says one of the team, Jessica Jimenez from Columbia University’s Vagelos College of Physicians & Surgeons.
Even more exciting is that we’ve already figured out a way of controlling these anxiety cells – in mice at least – to the extent it actually changes the animals’ observable behaviour.
Using a technique called optogenetics to shine a beam of light onto the cells in the vCA1 region, the researchers were able to effectively silence the anxiety cells and prompt confident, anxiety-free activity in the mice.
“If we turn down this activity, will the animals become less anxious?” Kheirbek told NPR.
“What we found was that they did become less anxious. They actually tended to want to explore the open arms of the maze even more.”
This control switch didn’t just work one way.
By changing the light settings, the researchers were also able to enhance the activity of the anxiety cells, making the animals quiver even when safely ensconced in enclosed, walled surroundings – not that the team necessarily thinks vCA1 is the only brain region involved here.
“These cells are probably just one part of an extended circuit by which the animal learns about anxiety-related information,” Kheirbek told NPR, highlighting other neural cells justify additional study too.
In any case, the next steps will be to find out whether the same control switch is what regulates human anxiety – and based on what we know about the brain similarities with mice, it seems plausible.
If that pans out, these results could open a big new research lead into ways to treat various anxiety conditions.
And that’s something we should all be grateful for.
“We have a target,” Kheirbek explained to The Mercury News. “A very early way to think about new drugs.”
What’s done is done.
What’s past is past.
Nothing to be done about it but learn from it.
And let it go.
Live confidently, fearlessly, positively.
Be sure of your success in everything you do.
Live with positive thoughts and gratitude.
With confidence, make the present the best it can be.
Enjoy the moment and savor and relish it
Have confidence that you can do it.
Look to the future with hope.
With confidence that you will make it good.
And know you will handle what comes your way with love and grace.
A daily dose of baking soda may help reduce the destructive inflammation of autoimmune diseases like rheumatoid arthritis, scientists say. They have some of the first evidence of how the cheap, over-the-counter antacid can encourage our spleen to promote instead an anti-inflammatory environment that could be therapeutic in the face of inflammatory disease, scientists report.
Pictured is Dr. Paul O’Connor, renal physiologist in the lab at the Medical College of Georgia Department of Physiology at Augusta University.
Credit: Phil Jones, Senior Photographer, Augusta University
A daily dose of baking soda may help reduce the destructive inflammation of autoimmune diseases like rheumatoid arthritis, scientists say.
They have some of the first evidence of how the cheap, over-the-counter antacid can encourage our spleen to promote instead an anti-inflammatory environment that could be therapeutic in the face of inflammatory disease, Medical College of Georgia scientists report in the Journal of Immunology.
They have shown that when rats or healthy people drink a solution of baking soda, or sodium bicarbonate, it becomes a trigger for the stomach to make more acid to digest the next meal and for little-studied mesothelial cells sitting on the spleen to tell the fist-sized organ that there’s no need to mount a protective immune response.
“It’s most likely a hamburger not a bacterial infection,” is basically the message, says Dr. Paul O’Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study’s corresponding author.
Mesothelial cells line body cavities, like the one that contains our digestive tract, and they also cover the exterior of our organs to quite literally keep them from rubbing together. About a decade ago, it was found that these cells also provide another level of protection. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed.
Drinking baking soda, the MCG scientists think, tells the spleen — which is part of the immune system, acts like a big blood filter and is where some white blood cells, like macrophages, are stored — to go easy on the immune response. “Certainly drinking bicarbonate affects the spleen and we think it’s through the mesothelial cells,” O’Connor says.
The conversation, which occurs with the help of the chemical messenger acetylcholine, appears to promote a landscape that shifts against inflammation, they report.
In the spleen, as well as the blood and kidneys, they found after drinking water with baking soda for two weeks, the population of immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. Macrophages, perhaps best known for their ability to consume garbage in the body like debris from injured or dead cells, are early arrivers to a call for an immune response.
In the case of the lab animals, the problems were hypertension and chronic kidney disease, problems which got O’Connor’s lab thinking about baking soda.
One of the many functions of the kidneys is balancing important compounds like acid, potassium and sodium. With kidney disease, there is impaired kidney function and one of the resulting problems can be that the blood becomes too acidic, O’Connor says. Significant consequences can include increased risk of cardiovascular disease and osteoporosis.
“It sets the whole system up to fail basically,” O’Connor says. Clinical trials have shown that a daily dose of baking soda can not only reduce acidity but actually slow progression of the kidney disease, and it’s now a therapy offered to patients.
“We started thinking, how does baking soda slow progression of kidney disease?” O’Connor says.
That’s when the anti-inflammatory impact began to unfold as they saw reduced numbers of M1s and increased M2s in their kidney disease model after consuming the common compound.
When they looked at a rat model without actual kidney damage, they saw the same response. So the basic scientists worked with the investigators at MCG’s Georgia Prevention Institute to bring in healthy medical students who drank baking soda in a bottle of water and also had a similar response.
“The shift from inflammatory to an anti-inflammatory profile is happening everywhere,” O’Connor says. “We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood.”
The shifting landscape, he says, is likely due to increased conversion of some of the proinflammatory cells to anti-inflammatory ones coupled with actual production of more anti-inflammatory macrophages. The scientists also saw a shift in other immune cell types, like more regulatory T cells, which generally drive down the immune response and help keep the immune system from attacking our own tissues. That anti-inflammatory shift was sustained for at least four hours in humans and three days in rats.
The shift ties back to the mesothelial cells and their conversations with our spleen with the help of acetylcholine. Part of the new information about mesothelial cells is that they are neuron-like, but not neurons O’Connor is quick to clarify.
“We think the cholinergic (acetylcholine) signals that we know mediate this anti-inflammatory response aren’t coming directly from the vagal nerve innervating the spleen, but from the mesothelial cells that form these connections to the spleen,” O’Connor says.
In fact, when they cut the vagal nerve, a big cranial nerve that starts in the brain and reaches into the heart, lungs and gut to help control things like a constant heart rate and food digestion, it did not impact the mesothelial cells’ neuron-like behavior.
The affect, it appears, was more local because just touching the spleen did have an effect.
When they removed or even just moved the spleen, it broke the fragile mesothelial connections and the anti-inflammatory response was lost, O’Connor says. In fact, when they only slightly moved the spleen as might occur in surgery, the previously smooth covering of mesothelial cells became lumpier and changed colors.
“We think this helps explain the cholinergic (acetylcholine) anti-inflammatory response that people have been studying for a long time,” O’Connor says.
Studies are currently underway at other institutions that, much like vagal nerve stimulation for seizures, electrically stimulate the vagal nerve to tamp down the immune response in people with rheumatoid arthritis. While there is no known direct connection between the vagal nerve and the spleen — and O’Connor and his team looked again for one — the treatment also attenuates inflammation and disease severity in rheumatoid arthritis, researchers at the Feinstein Institute for Medical Research reported in 2016 in the journal Proceedings of the National Academy of Sciences.
O’Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease.
“You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus,” he says, in this case, away from harmful inflammation. “It’s potentially a really safe way to treat inflammatory disease.”
The spleen also got bigger with consuming baking soda, the scientists think because of the anti-inflammatory stimulus it produces. Infection also can increase spleen size and physicians often palpate the spleen when concerned about a big infection.
Other cells besides neurons are known to use the chemical communicator acetylcholine. Baking soda also interact with acidic ingredients like buttermilk and cocoa in cakes and other baked goods to help the batter expand and, along with heat from the oven, to rise. It can also help raise the pH in pools, is found in antacids and can help clean your teeth and tub.
The research was funded by the National Institutes of Health.
A nasal spray formulation of ketamine shows promise in the rapid treatment of symptoms of major depression and suicidal thoughts, according to a new study published online today in The American Journal of Psychiatry (AJP).
The double-blind study compared the standard treatment plus an intranasal formulation of esketamine, part of the ketamine molecule, to standard treatment plus a placebo for rapid treatment of symptoms of major depression, including suicidality, among individuals at imminent suicide risk. The study involved 68 participants randomly assigned to one of two groups – either receiving esketamine or placebo twice a week for four weeks. All participants continued to receive treatment with antidepressants throughout. The researchers looked at effects at four hours after first treatment, at 24 hours and at 25 days.
The study was conducted by researchers at Janssen Research and Development and Janssen Scientific Affairs, Titusville, N.J., and San Diego, and the Yale School of Medicine, New Haven, Conn. They found a significant improvement in depression scores and decreased suicidal ideation in the esketamine group compared to the placebo group at four hours and at 24 hours. The esketamine effects were not greater than the placebo at 25 days. The measurement of suicide risk took into consideration both the patient’s and clinician’s perspectives.
The results of the study support nasal spray esketamine as a possible effective rapid treatment for depressive symptoms in patients assessed to be at imminent risk for suicide, according to the authors. Esketamine could be an important treatment to bridge the gap that exists because of the delayed effect of most common antidepressants. Most antidepressants take four to six weeks to become fully effective.
This study was a proof-of-concept, phase 2, study for esketamine; it must still go through a phase 3 study before possible FDA approval. It was funded by Janssen Research and Development, LLC.
The authors caution that more research is needed on the potential for abuse of ketamine. That caution is also the focus of an accompanying AJP editorial also published online today. In the editorial, AJP Editor Robert Freedman, M.D., along with members of the AJP Editorial Board, note the known potential for abuse and existing reports of abuse of prescribed ketamine. They discuss the need for additional research relating to the abuse potential of ketamine during phase 3 trials, such as monitoring of patients’ craving and potential ketamine use from other sources.
While it is the responsibility of physicians to provide a suicidal patient with the fullest range of effective interventions, the AJP Editor’s note, “protection of the public’s health is part of our responsibility as well, and as physicians, we are responsible for preventing new drug epidemics.” The Editors suggest the need for broad input in the development of effective controls on the distribution and use of ketamine.
Freedman and colleagues argue that steps to control the use of ketamine would not be aimed at preventing its use for beneficial purposes but would allow for treatment to “continue to be available to those with need, while the population that is at-risk for abuse is protected from an epidemic of misuse.”
This article has been republished from materials provided by American Psychiatric Association. Note: material may have been edited for length and content. For further information, please contact the cited source.
As my friend Sal pointed out, in order to come out of a depression or a manic phase, you have to seek/get help. And in the case of mental illness, because of the stigma, this requires courage. Well we have this courage.
If you broke your arm, you wouldn’t think twice about going to a doctor to get it repaired. You wouldn’t agonize over what the world will think of you if you admit you have a broken arm. You wouldn’t worry if someone saw the name of your medication, what would they think of you! You would simply march into the doctor’s office and get the treatment you needed.
Well, I know it’s very difficult to know that you are indeed in a depression the first time it hits you, but hopefully with the help of friends, family members, or doctors, when you do realize it is a depression, you don’t worry about the stigma, and go straight to a psychiatrist and get the help you need.
Depression, bipolar d/o, mental illness, is an illness of the brain, so it is a physical illness. And illnesses need to be treated to get better. So if you realize you are in a depression, march yourself to a good psychiatrist and get treatment. You are strong enough and you can get better, you will get better!
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